Background Young adults are now considered major spreaders of COVID-19 disease. Although most young individuals suffer from mild to moderate disease, there are concerns of long-term adverse health effects. The impact of COVID-19 disease and to which extent population-level immunity against SARS-CoV-2 exist in young adults remain unclear. Objective To conduct a population-based study on humoral and cellular immunity to SARS-CoV-2 and explore COVID-19 disease characteristics in young adults. Methods We invited participants from the Swedish BAMSE birth cohort (age 24-27 years) to take part in a COVID-19 follow-up. From 980 participants (October 2020-June 2021), we here present data on SARS-CoV-2 RBD-specific IgM, IgA and IgG titres measured by ELISA and on symptoms and epidemiological factors associated with seropositivity. Further, SARS-CoV-2-specific memory B- and T-cell responses were detected for a subpopulation (n=108) by ELISpot and Fluorospot. Results 28.4% of subjects were seropositive of which 18.4% were IgM single positive. One in seven seropositive subjects were asymptomatic. Seropositivity associated with use of public transport, but not with sex, asthma, rhinitis, IgE-sensitization, smoking or BMI. In a subset of representative samples, 20.7% and 35.0% had detectable SARS-CoV-2 specific B- and T-cell responses, respectively. B- and T-cell memory responses were clearly associated with seropositivity, but T-cell responses were also detected in 17.2% of seronegative subjects. Conclusion Assessment of IgM and T-cell responses may improve population-based estimations of SARS-CoV-2 infection. The pronounced surge of both symptomatic and asymptomatic infections among young adults should imply a continuation of the large-scale vaccination campaign.

Simultaneously elevated FeNO and B-Eos related to reduced lung function in asthmatics, wheezing symptoms, but not to a history of asthma attacks. Asthma attacks and ER-visit due to asthma were related to increased B-Eos levels.

Purpose of review Finding suitable biomarkers to phenotype asthma, identify individuals at risk of worsening and guide treatment is highly prioritized in asthma research. We aimed to provide an analysis of currently used and upcoming biomarkers, focusing on developments published in the past 2 years. Recent findings Type 2 inflammation is the most studied asthma mechanism with the most biomarkers in the pipeline. Blood eosinophils and fractional exhaled nitric oxide (FeNO) are those most used clinically. Recent developments include their ability to identify individuals at higher risk of exacerbations, faster decline in lung function and more likely to benefit from anti-IL-5 and anti-IL-4/-13 treatment. Certain patterns of urinary eicosanoid excretion also relate to type 2 inflammation. Results of recent trials investigating the use of serum periostin or dipeptidyl peptidase-4 to guide anti-IL-13 therapy were somewhat disappointing. Less is known about non-type 2 inflammation but blood neutrophils and YKL-40 may be higher in patients with evidence of non-type 2 asthma. Volatile organic compounds show promise in their ability to distinguish both eosinophilic and neutrophilic asthma. Summary The ultimate panel of biomarkers for identification of activated inflammatory pathways and treatment strategies in asthma patients still lies in the future, particularly for non-type 2 asthma, but potential candidates are available.

FeNO and S-ECP are markers for inflammation in asthma, but are dependent on different inflammatory pathways and weakly correlated. Simultaneous measurements of both offer better risk characterization of adult asthmatics.

Background: Some asthmatics develop irreversible chronic airflow obstruction, for example, fixed airflow obstruction (fixed-AO). This is probably a consequence of airway remodelling, but neither its relation to inflammation nor which asthma biomarkers can be clinically useful are elucidated. We hypothesized that the presence of type 2 inflammation relates to fixed-AO. Objectives:To evaluate the presence of four markers for type 2 inflammation in fixed airflow obstruction among asthmatics.Methods: This was a cross-sectional study of 403 participants with asthma, aged 17-75 years, from three Swedish centres. Fixed airflow obstruction was defined as forced expiratory volume during the first second (FEV 1 ) over forced vital capacity (FVC) being below the lower limit of normal (LLN). The following type 2 inflammation markers were assessed: exhaled nitric oxide (FeNO), serum periostin, serum eosinophil cationic protein (S-ECP), and urinary eosinophil-derived neurotoxin (U-EDN).Results: Elevated U-EDN (values in the highest tertile, ≥65.95 mg/mol creatinine) was more common in subjects with fixed-AO vs. subjects without fixed-AO: 55% vs. 29%, P < 0.001. Elevated U-EDN related to increased likelihood of having fixed-AO in both all subjects and never-smoking subjects, with adjusted (adjusted for sex, age group, use of inhaled corticosteroids last week, atopy, early-onset asthma, smoking history, and packyears) odds ratios (aOR) of 2.38 (1.28-4.41) and 2.51 (1.04-6.07), respectively. In a separate analysis, having both elevated S-ECP (>20 μg/L) and U-EDN was related to having the highest likelihood of fixed-AO (aOR (95% CI) 6.06(2.32-15.75)). Elevated serum periostin or FeNO did not relate to fixed-AO. Conclusions and clinical relevance:These findings support that type 2 inflammation, and in particular eosinophil inflammation, is found in asthma with fixed-AO.This could indicate a benefit from eosinophil-directed therapies. Further longitudinal studies are warranted to investigate causality and relation to lung function decline.